The phenomena of head injury is well described in "Intensive Management of Severe Head Injury", Borel et al, CHEST, July, 1990, pages 180-189, at page 181. Cerebral injuries may be of either the penetrating or non-penetrating varieties, both of which cause damage to the brain and vasculature structures. Secondary injury to the brain indicates a vicious circle of escalating injury. Cerebral injury causes cerebral edema, cerebral edema raises intracranial volume which increases intracranial pressure, raised intracranial pressure compresses brain tissue and decreases cerebral perfusion pressure further increasing cerebral injury. Decreases in cerebral perfusion pressure result in cerebral blood flow falling below the level necessary to prevent neurologic ischemia and cell injury. When compartmental pressure gradients are established by local areas of injury, transcompartmental herniation of brain tissue results in catastrophic neurologic injury.
Nutritional support of the patient with a neurological injury is a complex problem. Patients with a severe head injury are hypermetabolic and catabolic, and they require early and intensive nutritional support to minimize malnutrition-related complications. Nutritional support may, however, adversely affect neurological recovery. Experimental studies have shown that hyperglycemia due to glucose infusion or to the postprandial state worsens neurological recovery from cerebral and spinal cord ischemia. The mechanism of this detrimental effect is not completely understood, however, in many studies hyperglycemia has been associated with increased accumulation of lactic acid. Development of a diet which would supply protein and caloric needs without adversely affecting neurological recovery would have widespread use in patients with central nervous system ischemia or trauma.
Glucose tolerance of critically ill patients receiving nutritional support is an important concern of nutritional support personnel. Several studies have demonstrated that injured and critically ill patients have increased rates of glucose production and glucose oxidation which are not easily suppressed by exogenous glucose administration. It has been demonstrated that accelerated gluconeogenesis can not be reduced by administration of exogenous glucose at rates which would normally suppress glucose production. Very high levels of blood glucose can result with the administration of an exogenous source of carbohydrate because the patient is in a persistent gluconeogenic state and has a blunted insulin response, a decreased tissue sensitivity to insulin and/or an impaired peripheral utilization of glucose.
As with critically ill patients in general, hyperglycemia is frequently associated with severe head injury. In the course of alimenting patients with a severe head injury, the hyperglycemic response can be exaggerated by the feeding of conventional alimentation formulas which use glucose as the major nonprotein caloric source. Hyperglycemia has been associated with poor neurological outcome. The late neurological sequelae of cerebral ischemia are consistently worse when the blood glucose level is elevated during ischemia, suggesting that lactic acidosis or other metabolic consequences of glucose metabolism damages nervous tissue.
Fasting has been used as a means to reduce blood glucose following head injury. However, it has been reported that malnutrition can lead to suppression of immune responses and poor wound healing. Also, failure to treat the hypermetabolic response in head injury is probably undesirable, since head-injury deaths are often due to infection, which could be related to malnutrition. Previous studies have suggested that alimentation with nonglucogenic (not converted to glucose in the body) energy substrates, such as ketone bodies, may have a less detrimental effect on neurological recovery from ischemia than alimentation with glucose Peek et al., "Ketone precursors as nutritional substrates may improve neurological outcome following ischemia", Journal of Neurotrauma, 1989 6:205-206.
Considering the negatives associated with fasting, there is a need for a nutritional product which will provide nutritional support after injury, yet not exaggerate the hyperglycemic response after injury. A nutritional product in accordance with the present invention: (a) is very low in, preferably free of, carbohydrate; (b) contains a lipid blend formulated to minimize the hypermetabolic response and reduce the frequency of ischemic events after severe head injury; and (c) an antioxidant system that restores antioxidant status in a head trauma patient and prevents or minimizes peroxidation of highly unsaturated fatty acids in the lipid blend.